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Biomedical subjects

H L Brooks

Publications and source records attributed to H L Brooks.

At least 73 records · Page 4Linked to original sources
PubMed1984

Long-term survival after prehospital sudden cardiac death.

One hundred thirty-nine survivors of prehospital sudden cardiac death were followed after their hospital discharge. Eighty patients were studied with coronary angiography and cardiac catheterization; 34 of these underwent coronary bypass surgery. After a maximum follow-up of 105 months, 89 patients were still alive. The probability of survival at 6 months, 1 year, 2 years, 3 years, 4 years, and 5 years was 88%, 86%, 78%, 70%, 63%, and 59%, respectively. Of the 43 cardiac deaths, 37 (86%) were secondary to documented recurrent ventricular fibrillation or occurred suddenly. Twelve percent of the total population had recurrent ventricular fibrillation in the first year following the initial cardiac arrest, 16% within 2 years, and 22% within 3 years. Of the 37 survivors dying from recurrent ventricular fibrillation, 32% died within the first 3 months following hospital discharge, 46% in the first year, 64% within 2 years, and 78% within the first 3 years. Most survivors were capable of resuming normal activities after hospital discharge. Only 7% demonstrated permanent neurologic impairment. Sixty-eight percent of the patients who were employed at the time of their prehospital sudden cardiac arrest returned to full-time employment. In the subset of 34 surgically treated patients, there have been six (18%) cardiac deaths. Four of these deaths were related to recurrent ventricular fibrillation, with one of these deaths occurring in the immediate postoperative period. The other three deaths related to recurrent ventricular fibrillation occurred 36 months (two deaths) and 49 months following the initial prehospital cardiac arrest.

Adolescent↗
PubMed1984

Contrasting effects of pharmacologic vasodilation on true collateral and overlap perfusion in ischemic myocardium.

The effects of chromonar (3.5 and 7.0 mg/kg i.v.), a selective coronary vasodilator, on true collateral blood flow and overlap flow (noncollateral perfusion due to overlapping end arteries of adjacent coronary vessels) were measured independently in anesthetized dogs following acute coronary occlusion. Collateral flow in the ischemic zone was significantly (P less than 0.05) reduced by chromonar in a dose-related manner while transmural overlap flow was increased. True collateral flow was distributed primarily to the subepicardium and chromonar produced a significant reduction in both subepicardial and subendocardial perfusion. Overlap perfusion was distributed equally across the left ventricular wall and chromonar increased perfusion to both subepicardium and subendocardium. The results indicate that there are two independent sources of perfusion of ischemic myocardium and that pharmacologic vasodilation with chromonar produces opposite effects on each: a steal of true collateral blood flow and an increase in overlap perfusion.

Animals↗
PubMed1984

Changes in circulating blood volume influence aortic characteristic impedance in awake dogs.

Experiments on five chronically instrumented dogs were performed to study the effects of changes in circulating blood volume on the aortic smooth muscle activity in awake animals. The external diameter of the proximal descending aorta was measured with a sonomicrometer. Aortic pressure was measured in the same cross-sectional area with a catheter-tip transducer. Acute hemorrhage of 15% of the estimated blood volume was performed 17 times by quickly withdrawing blood through a jugular cannula. At any given arterial pressure within the range of overlap the aortic diameter (D) was always decreased after hemorrhage compared with control, and the pressure-strain elastic modulus (Ep) and the characteristic impedance (Zc) were always increased. For example at 140 kdyn X cm-2 (104.5 mmHg) delta D = -0.61 +/- 0.12 mm or delta D = -3.44 +/- 0.68% of control, delta Ep = 31.0 +/- 8.6%, and delta Zc = 22.6 +/- 4.5%. Each of these changes was significant with P less than 0.01. Volume expansion of 30% was performed eight times by infusing warm saline. At any given arterial pressure D was always increased and Ep and Zc were always decreased. At 140 kdyn X cm-2 delta D = 0.55 +/- 0.15 mm or delta D = 3.12 +/- 0.95% of control, delta Ep = -12.4 +/- 3.2%, and delta Zc = -12.0 +/- 2.1%. Each of these changes was significant with P less than 0.01. Since in these awake animals the changes in circulatory blood volume modified the arterial pressure only slightly, the contribution of viscoelasticity and myogenicity to the observed responses was minimal.

Animals↗
PubMed1984

Right ventricular and right atrial collapse in patients with cardiac tamponade--a combined echocardiographic and hemodynamic study.

To determine the hemodynamic derangement associated with right ventricular diastolic collapse and to assess the value of right ventricular and right atrial collapse in identifying cardiac tamponade, two-dimensional echocardiograms were recorded simultaneously with measurement of right atrial, pulmonary capillary wedge, intrapericardial, and systemic arterial pressures and cardiac output in 16 patients as they underwent pericardiocentesis. Twelve patients (group I) had evidence of right ventricular or right atrial collapse or both on their echocardiograms and hemodynamic evidence of cardiac tamponade before pericardiocentesis. All hemodynamic parameters improved after pericardiocentesis (p less than or equal to .05). Continuous monitoring during pericardiocentesis in three of these patients showed significant improvement in all parameters except heart rate (p less than or equal to .02) at the point of disappearance of right ventricular diastolic collapse, with further improvement in cardiac output as pericardiocentesis continued (p less than .01). Right atrial collapse persisted after right ventricular collapse disappeared but was no longer present when pericardiocentesis was completed. Three patients (group II) had no right ventricular or right atrial collapse, no hemodynamic evidence of cardiac tamponade, and no improvement in hemodynamic parameters after pericardiocentesis. A single patient (group III) was found to have elevated right heart pressures and right ventricular hypertrophy before pericardiocentesis. Although there was hemodynamic evidence of cardiac tamponade in this patient, there was no evidence of right ventricular or right atrial collapse. In this study, the sensitivity of right ventricular collapse as a marker for cardiac tamponade was 92%, its specificity 100%, its accuracy 94%, and its predictive value 100%.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Comparative actions of dihydropyridine slow channel calcium blocking agents in conscious dogs: systemic and coronary hemodynamics with and without combined beta adrenergic blockade.

The cardiovascular effects of the dihydropyridine slow channel calcium blocking agents, nifedipine, nitrendipine, FR 34235, niludipine and nisoldipine were compared to the vasodilator, hydralazine, in conscious, instrumented dogs before and after propranolol (2 mg/kg i.v.). The calcium-blocking agents (1.0, 2.5, 5.0, 10.0 and 25.0 micrograms/kg/min i.v.) and hydralazine (0.01, 0.025, 0.05, 0.10 and 0.25 mg/kg/min i.v.) produced dose-related decreases in blood pressure and reflex increases in heart rate and heart rate-systolic pressure product, an index of myocardial oxygen consumption. Hydralazine also produced a reflex increase in myocardial contractility (+dP/dt); however, minimal changes in contractility were observed with the dihydropyridines. Nisoldipine, nitrendipine and FR 34235 were relatively more effective in reducing arterial pressure than niludipine, nifedipine and hydralazine. For any given reduction in pressure, hydralazine produced the greatest reflex tachycardia at low doses. Of the calcium channel blockers, nifedipine produced the greatest and niludipine the least reflex tachycardia. Propranolol attenuated the reflex increase in heart rate and rate-pressure product produced by all vasodilators studied. Only slight changes in global contractility were observed after combined use of the dihydropyridines and propranolol. Nisoldipine, FR 34235 and nifedipine produced the greatest coronary vasodilation whereas niludipine, nitrendipine and hydralazine were less effective. In addition, the dihydropyridines produced a greater increase in systolic than diastolic flow. The present results demonstrate that while all dihydropyridine calcium channel blocking agents exhibit many similarities, certain differences exist. Furthermore, the "reflex" tachycardia observed with these drugs was not solely related to the degree of reduction in arterial pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1984

Comparative actions of dihydropyridine slow channel calcium blocking agents in conscious dogs: alterations in baroreflex sensitivity.

The effects of five dihydropyridine slow channel calcium blocking agents, nifedipine, nitrendipine, FR 34235, niludipine and nisoldipine were compared to those of the peripheral vasodilator hydralazine on the reflex bradycardia and tachycardia after abrupt increases and decreases in arterial pressure in conscious dogs. On alternate days, the baroreflex was elicited during control conditions (drug vehicle) and/or after low (2.5 micrograms/kg/min) or high (5.0 micrograms/kg/min) equihypotensive doses of calcium antagonists or hydralazine (0.05 and 0.1 mg/kg/min). Baroreflexes were elicited by means of bolus injection of nitroprusside and phenylephrine. Certain of the dihydropyridine calcium channel blocking agents were found to interfere significantly with the reflex bradycardia after a rise in pressure, a phenomenon usually attributed to an increase in parasympathetic tone. Nisoldipine, niludipine and FR 34235 decreased baroreceptor sensitivity (defined as delta cardiac interval/delta systolic arterial pressure; milliseconds per millimeter of mercury) in a dose-related manner. On the other hand, nifedipine, nitrendipine and hydralazine had no significant effect. The dihydropyridines and hydralazine had little effect on baroreceptor-induced withdrawal of vagal tone or increases in sympathetic tone in response to sudden decreases in blood pressure. Calcium antagonists with isopropyl substitution as part of the ester function on the dihydropyridine nucleus, nisoldipine, niludipine and FR 34235, interfered to a greater extent with the vagally mediated reduction in cardiac rate. Changes in baroreflex gain may provide a basis for differential actions of dihydropyridine calcium channel blockers on the magnitude of change in heart rate in response to an abrupt increase in arterial pressure.

Animals↗
PubMed1983

Coronary hemodynamics and subendocardial perfusion distal to stenoses.

We compared distal coronary hemodynamics and regional myocardial perfusion in anesthetized dogs in the presence of a single or two coronary artery stenoses in series. After application of either a single or two stenoses on the left anterior descending coronary artery, regional myocardial blood flow was measured with radioactive microspheres. Moderate degrees of single-vessel stenosis (no change in resting coronary blood flow but reduction in reactive hyperemic response of 70%) resulted in no significant change in regional myocardial perfusion at rest despite a pressure drop across the stenosis of 24 +/- 3 mm Hg. When two such stenoses were applied in series, there was a 91% decrease in reactive hyperemia, a significant reduction in resting diastolic coronary blood flow and a 51 +/- 7 mm Hg pressure drop across the two stenoses. Alone, each stenosis produced no change in regional myocardial perfusion; however, together the two stenoses resulted in a significant decrease in subendocardial blood flow and a redistribution of transmural perfusion within the ischemic zone favoring the subepicardium (endo/epi from 0.95 +/- 0.03 to 0.72 +/- 0.03). The results indicate that whereas resting subendocardial perfusion is not significantly affected by moderate degrees of a single coronary artery stenosis, multiple stenoses of the same severity may dramatically reduce subendocardial perfusion.

Animals↗
PubMed1983

Out-of-hospital pulmonary edema: diagnosis and treatment.

Sixty-two patients diagnosed by paramedics as having acute cardiac pulmonary edema out of the hospital were studied. The paramedic prehospital diagnosis as confirmed by an emergency physician, chest film, and hospital admission evaluation was correct in 55 of 62 patients (89%). In the group with acute cardiac pulmonary edema, 64% demonstrated cardiac dysrhythmias, including cardiac arrest, prior to the patient's hospitalization. Therapy administered by the paramedics was beneficial in that most patients had improved on arrival at the hospital. Six of the 10 patients (60%) sustaining cardiac arrest were successfully resuscitated. Acute cardiac pulmonary edema occurring outside the hospital is commonly associated with significant complications, including life-threatening arrhythmias. Well-trained paramedics are capable of quickly diagnosing and treating acute cardiac pulmonary edema outside the hospital setting.

Adult↗
PubMed1983

Radiation hazards in scoliosis management.

Safe radiography in scoliosis management is based on a sound knowledge of 1) the radiographic imaging process, 2) the degree of risk to the patient from radiation exposure, and 3) the radiographic requirements to both evaluate and follow patients with spine deformity. This paper is a current review of the subject and work done at the authors' centers. It includes recommendations for reducing the radiation risk while maintaining necessary diagnostic information.

Child↗
PubMed1983

Effects of histamine receptor stimulation on regional myocardial blood flow.

The effect of histamine (H) and specific H1 and H2 agonists and antagonists on regional myocardial blood flow was studied in anesthetized dogs by use of tracer microspheres. Intracoronary infusion of histamine (15 and 34 micrograms/min) produced a dose-related increase in transmural myocardial blood flow (from 0.82 to 1.36 and 2.25 ml X min-1 X g-1) without alteration of heart rate or blood pressure. Infusion of the H1 agonist 2-(2-thiazolyl)ethylamine (135 and 442 micrograms/min) produced an increase in transmural perfusion (from 0.69 to 1.22 and 1.65 ml X min-1 X g-1) and a significant (P less than 0.05) increase in the ratio of flow between subendocardium and subepicardium (endo/epi from 0.97 to 1.31 and 1.54). Infusion of the H2 agonist dimaprit (195 and 390 micrograms/min) produced an increase in transmural myocardial blood flow (from 0.97 to 1.49 and 2.00 ml X min-1 X g-1) without a change in endo/epi. The H1-mediated increase in regional myocardial perfusion and endo/epi was blocked by the H1 antagonist diphenhydramine but not by the H2 antagonist cimetidine. These results suggest that stimulation of H1 coronary receptors preferentially distributes flow to the subendocardium, whereas H2 receptors mediate vasodilation in subepicardium as well as subendocardium.

Animals↗
PubMed1983

The hemodynamic derangement associated with right ventricular diastolic collapse in cardiac tamponade: an experimental echocardiographic study.

Clinical reports indicate that right ventricular diastolic collapse (RVDC) is associated with cardiac tamponade. To assess the hemodynamic abnormalities associated with RVDC, we studied six chronically instrumented conscious dogs (group A) with two-dimensional echocardiography during cardiac tamponade induced by continuous saline infusion into the pericardial space. We recorded cardiac output (electromagnetic flowmeter), heart rate, respiration, and aortic, intrapericardial, and right atrial pressures. In four additional animals (group B), we recorded right ventricular pressure and placed a hydraulic occluder around the pulmonary artery so that short-term reversible obstruction to right ventricular outflow could be produced. None of the dogs had RVDC when the pericardial space was empty, but all dogs showed RVDC during cardiac tamponade. The appearance of RVDC in group A was associated with a 21% reduction in cardiac output (p less than .01) and no change in mean aortic pressure. Short-term partial pulmonary artery obstruction led to increased right ventricular pressures and a striking reduction in RVDC in early tamponade, suggesting that RVDC is caused by pericardial pressure exceeding right ventricular pressure in early diastole. An additional animal had right ventricular hypertrophy caused by a severe "heart worm" infestation and did not show RVDC during cardiac tamponade. These observations suggest that in the absence of increased resistance to right ventricular outflow or right ventricular hypertrophy, RVDC occurs early in the course of cardiac tamponade and is associated with a hemodynamically important decrease in cardiac output.

Animals↗
PubMed1983

Misdiagnosis of pericardial cyst by echocardiography and computed tomography scanning.

We saw a patient who had clinical features of right-sided heart failure. Echocardiography and computed tomography findings were incorrectly interpreted as demonstrating an intracardiac mass. At surgery, a pericardial cyst externally compressing the right ventricular cavity was found. We conclude that, although noninvasive tests may play a valuable role in evaluating intracardiac masses, interpretation may be difficult and misdiagnoses are possible.

Aged↗
PubMed1982

Beneficial effects of the dihydropyridine calcium antagonist, FR 34235, in a chronic coronary occlusion model.

Administration of FR 34235 reduced aortic blood pressure and increased cardiac output in anesthetized dogs with an ameroid-induced coronary artery occlusion. Following FR 34235, there was an increase in perfusion within normal myocardium and ischemic subepicardium. Ischemic zone flow to subepicardium and subendocardium were both significantly increased when aortic pressure was held at control levels. The data demonstrate marked enhancement in oxygen supply to an area distal to a chronic coronary occlusion by a new calcium antagonist, FR 34235.

Animals↗
PubMed1982

Evaluation of postresuscitation left ventricular global and segmental function by radionuclide ventriculography in sudden coronary death survivors of prehospital cardiac arrest: Correlation to subsequent short-term prognosis.

Previous data have shown that patients with significant left ventricular (LV) dysfunction, marked abnormalities in resting hemodynamics, and multiple vessel coronary artery disease (CAD) are at increased risk for sudden cardiac death. However, in-hospital assessment of ventricular function in the early postresuscitation period of out-of-hospital cardiac arrest has not been evaluated and related to short-term outcome. By using bedside radionuclide ventriculography (RNV) we evaluated LV ejection fraction (LVEF) and wall motion in 36 nonconsecutive patients within 24 hours of their episode of out-of-hospital cardiac arrest. There were 24 men and 12 women with mean age of 62.3 years (range 21 to 85 years). Total mortality of the entire group was 38.8% at 4 weeks. Eighteen patients had LVEF less than 0.30 and 18 had LVEF greater than 0.30. Mortality in the low LVEF group was 55.5% at 4 weeks versus 22.2% in patients with LVEF greater than 0.30 (p less than 0.05). Patients with normal LV wall motion had no short-term mortality (none of seven), while patients having abnormal LV wall motion had a significantly higher short-term mortality (14 of 29) (p less than 0.05). We conclude that out-of-hospital cardiac arrest survivors have a high incidence of severe LV dysfunction in the early postresuscitation period and that a significantly higher early mortality is seen in the group with LVEF less than 0.30. In addition, abnormalities of LV wall motion by RNV examination demonstrated poorer prognosis in the first 4 weeks than patients with normal LV wall motion.

Adult↗
PubMed1982

Subendocardial versus transmural myocardial infarction: relationship to the collateral circulation in canine and porcine hearts.

In the present study, the relationship between transmural perfusion gradients and myocardial infarct size and distribution in canine and porcine hearts was characterized. Anesthetized pigs (N = 6) and dogs (N = 7) underwent a 2-h occlusion and 5-h reperfusion of the distal third of the left anterior descending coronary artery. The area at risk for infarction and ultimate infarct size were determined by fluorescein dye infused intracoronary and nitro blue tetrazolium stain, respectively. Myocardial perfusion within normal, ischemic, and infarcted regions was determined by the radioactive microsphere technique in each species. In dogs, infarction was subendocardial and comprised 29.9 +/- 5.5% of the area at risk, while in pigs infarction was transmural and comprised 50.1 +/- 4.2% (p less than 0.05). Collateral perfusion of the subendocardium of infarcted regions in pig and dog hearts was similar (0.05 mL X min-1 X g-1), while flow to the subepicardium was significantly (p less than 0.05) higher in dogs than in pigs (0.25 versus 0.05 mL X min-1 X g-1). The data demonstrate that species differences in myocardial infarct size and shape are related to differences in coronary collateral blood flow. The smaller subendocardial infarction in dog hearts is related to a relatively high subepicardial perfusion and transmural infarction in pig hearts owing to the lack of collateral perfusion in subepicardium as well as subendocardium.

Animals↗
PubMed1982

Myocardial perfusion distal to an acute or chronic coronary artery occlusion: effects of diltiazem and nifedipine.

The effect of two slow channel calcium antagonists, diltiazem and nifedipine, on perfusion of normal and ischemic myocardium was studied in anesthetized dogs with acute or chronic (ameroid constrictor) left anterior descending coronary artery occlusion. Diltiazem (15 and 30 micrograms/mkg/min i.v.) produced significant (P less than .05) and dose-related decreases in heart rate and mean aortic blood pressure and an increase in left circumflex coronary blood flow. Nifedipine (1 and 3 micrograms/kg/min i.v.) also produced a significant reduction in mean aortic blood pressure and an increase in left circumflex coronary artery blood flow; however, no change in heart rate was observed. Both diltiazem and nifedipine increased myocardial blood flow in the normal zone in dogs with acute or chronic coronary artery occlusion, and this effect was potentiated when aortic blood pressure was prevented from decreasing. Following a reduction in aortic blood pressure no significant change in ischemic zone perfusion was observed after diltiazem in dogs with an acute occlusion; flow was significantly increased in dogs with a chronic occlusion. In both models, diltiazem produced a redistribution of ischemic zone blood flow to the subendocardium. In dogs with acute or chronic occlusion nifedipine produce an increase in ischemic zone flow primarily to the subepicardium. The effect of each agent on tissue perfusion was enhanced in the chronic occlusion model. These data demonstrate marked differences in effects of diltiazem and nifedipine on hemodynamics and regional myocardial perfusion and stress the importance of experimental models in evaluating the effects of the calcium antagonists on coronary collateral blood flow.

Acute Disease↗